Amongthe non-communicable diseases, atherosclerotic heart disease is considered a
major health hazard in our country leading to increase morbidity and mortality.
Atherosclerosis is regarded as a dynamic and progressive disease arising from
the combination of endothelial dysfunction and inflammation. The classic
concept of atherosclerosis as a disorder of lipid metabolism and deposition has
gained wide acceptance. However, the story of atherogenesis extends beyond
dyslipidemia.
Inrecent years, scientists have shown that inflammation is involved in the
initiation (atherogenesis), lesion progression and ultimate complications
leading to acute coronary and cerebrovascular catastrophes due to complications
like plaque rupture, intra plaque hemorrhage and thromboembolism. The factors
leading to the instability of a plaque includes increased accumulation of lipid,
the thinness of the fibrous cap and local inflammation.
Therole of inflammation in atherosclerosis has been studied to a great extent in
recent years and is considered a major factor for plaque vulnerability.
Inflammatory mediators like cytokines promote the migration and proliferation
of smooth muscle cells leading to their transformation into foam cells.
Inflammation also leads to increased neo-vascularization of the plaque. There
is need to study the immunohistochemical markers of macrophages and smooth
muscle
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